Background and objectivesNative kidney biopsies are commonly performed in the diagnosis of acute kidney diseases and CKD. Because of the invasive nature of the procedure, bleeding-related complications are not uncommon. The National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases–sponsored Kidney Precision Medicine Project requires that all participants undergo a kidney biopsy; therefore, the objective of this analysis was to study complication rates of native kidney biopsies performed using automated devices under kidney imaging.Design, setting, participants, & measurementsThis is a systematic review and meta-analysis of the literature published from January 1983 to March 2018. The initial PubMed search yielded 1139 manuscripts. Using predetermined selection criteria, 87 manuscripts were included in the final analysis. A random effects meta-analysis for proportions was used to obtain combined estimates of complication rates. Freeman–Tukey double-arcsine transformations were used to stabilize variance as complications were rare.ResultsA total of 118,064 biopsies were included in this study. Patient age ranged from 30 to 79 years, and 45% of patients were women. On the basis of our meta-analysis, pain at the site of biopsy is estimated to occur in 4.3% of biopsied patients, hematomas are estimated to occur in 11%, macroscopic hematuria is estimated to occur in 3.5%, bleeding requiring blood transfusions is estimated to occur in 1.6%, and interventions to stop bleeding are estimated to occur in only 0.3%. Death attributed to native kidney biopsy was a rare event, occurring only in an estimated 0.06% of all biopsies but only 0.03% of outpatient biopsies. Complication rates were higher in hospitalized patients and in those with acute kidney disease. The reported complications varied on the basis of study type and geographic location.ConclusionsAlthough the native kidney biopsy is an invasive diagnostic procedure, the rates of bleeding complications are low. Albeit rare, death can occur postbiopsy. Complications are more frequently seen after kidney biopsies of hospitalized patients with AKI.
In this article, the pathophysiology of left ventricular failure is reviewed. By contrast, the paucity of information about pulmonary arterial hypertension and right ventricular failure is acknowledged. The potential mechanisms whereby renal sodium and water retention in right ventricular failure secondary to pulmonary arterial hypertension can occur, despite normal left ventricular function, are discussed. With right ventricular failure as the primary cause of death in patients with pulmonary hypertension, more information about the mechanisms of renal sodium and water retention in these patients is direly needed. Specifically, studies to examine the activation of the neurohumoral axis at various stages of pulmonary arterial hypertension and right ventricular failure, including inhibition of mineralocorticoid and V2 vasopressin receptors, are indicated. Clin J Am Soc Nephrol 3: 1232-1237. doi: 10.2215 T he renal sodium and water retention that occurs with advanced left ventricular failure is associated with substantial morbidity and mortality. This sodium and water retention, which can lead to pulmonary edema, pleural effusion, and peripheral edema, occurs despite an increase in total blood volume. In normal individuals, a rise in total blood volume increases renal sodium and water excretion. The kidney is intrinsically intact with left ventricular failure, because the renal sodium and water retention does not persist after a successful heart transplant.This seeming paradox of increased blood volume yet renal sodium and water retention in cardiac failure has been explained by the body fluid volume regulation hypothesis (1-3). This hypothesis proposes that the kidney does not respond to changes in total blood volume but rather responds to what has been termed effective arterial blood volume. In general terms, approximately 85% of circulating blood volume is in the lowpressure venous side of the circulation, whereas only 15% is in the high-pressure arterial circulation. The integrity of the arterial circulation depends on cardiac output and systemic vascular resistance and is modulated by arterial stretch baroreceptors in the carotid sinus, aortic arch, and afferent arteriole of the glomerulus (4). Thus, despite an increase in total blood volume, arterial underfilling can occur secondary to a decrease in cardiac output in low-output heart failure or decreased systemic vascular resistance in high-output heart failure. With arterial underfilling secondary to either condition, arterial baroreceptor-mediated activation of the neurohumoral axis occurs. The resultant increase in renin-angiotensin-aldosterone system (RAAS) leads to sodium retention, and the increase in the nonosmotic release of arginine vasopressin (AVP) is associated with water retention and hyponatremia in advanced left ventricular failure, a known risk factor for increased mortality (5). This water retention is due to AVP activation of the V2 vasopressin receptors on the basolateral surface of the principal cells of the collecting duct, which increas...
Understanding kidney disease relies on defining the complexity of cell types and states, their associated molecular profiles and interactions within tissue neighbourhoods1. Here we applied multiple single-cell and single-nucleus assays (>400,000 nuclei or cells) and spatial imaging technologies to a broad spectrum of healthy reference kidneys (45 donors) and diseased kidneys (48 patients). This has provided a high-resolution cellular atlas of 51 main cell types, which include rare and previously undescribed cell populations. The multi-omic approach provides detailed transcriptomic profiles, regulatory factors and spatial localizations spanning the entire kidney. We also define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive (successful or maladaptive repair), transitioning and degenerative states. Molecular signatures permitted the localization of these states within injury neighbourhoods using spatial transcriptomics, while large-scale 3D imaging analysis (around 1.2 million neighbourhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways that are relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents a comprehensive benchmark of cellular states, neighbourhoods, outcome-associated signatures and publicly available interactive visualizations.
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